Effects of Deficiency of Vitamin A. Much research has been done on the effects of deprivation of animals of this vitamin. The injury to the body which results from this kind of specific starvation is limited to the epithelial tissues. Since these line the ducts of the tear glands, salivary glands, and other digestive glands, and constitute other glandular tissues of major importance, vitamin A deficiency quickly undermines health. The epithelial cells keratinize, becoming like the outer layers of the skin, and lose their normal functions. Plaques of these cells desquamate and tend to plug the ducts of glands. In vitamin A deficiency the earliest symptoms are deficiency of tears, dryness of the eyes, and dryness of the mouth. The skin becomes dry and scaly, the germinal epithelium in the testes degenerates, and the animals become sterile.

Attention has repeatedly been called to the occurrence of large numbers of calculi in the kidneys and bladders of rats suffering from deficiency of vitamin A. Rats develop deposits of phosphates and oxalates in the urinary tract very rapidly, and almost invariably when fed diets deficient in this vitamin. When chickens are fed an A-deficient diet, there accumulate in the kidneys great numbers of crystals of urates, or salts of uric acid, so that the kidneys feel sandy between the fingers. There is also some evidence that gall stones are more likely to develop under conditions of vitamin A insufficiency than otherwise. Plaques of epithelial cells desquamate and form nuclei upon which cholesterol deposits.

One of the earliest observed effects of vitamin A deficiency was the appearance of an ophthalmia characterized by drying of the cornea followed by ulceration and perforation of the eyeball. This has been shown to be a secondary result of injury to the tear glands. The gland atrophies and loses its power to secrete tears; the eyeball thereupon becomes dry, and cornification of the cornea soon develops.

A number of papers have been published which refer to the incidence of a similar ophthalmia in human subjects subsisting upon diets of poor quality. There is much reason to believe that the occurrence of night blindness is sometimes attributable to chronic deficiency of vitamin A. In the intestinal tract there may be impaired absorption due to injury to the epithelial cells of the wall.

In rats, when the diet is impoverished in vitamin A, the vaginal mucosa forms cornified epithelial cells continuously. Under normal nutrition there is a similar cornification limited to a brief period during which there is growth, maturation, and rupture of Graafian follicles, after which it disappears; but in A-deficient rats the desquamation of cornified cells is continuous and obscures all ovarian cycles that may be present. Vitamin A deficiency does not create a malfunction of the ovaries, for they continue to secrete hormones similar to those in estrus. This effect on the vaginal mucosa of the rat is so pronounced that Evans and Bishop report their ability to detect vitamin A deficiency in otherwise apparently healthy animals receiving enough A to prevent ophthalmia. Raising the level of A in the diet may abolish the persistent cornification of the vaginal epithelium and restore normal conditions.

In vitamin A deficiency this transformation of epithelium into stratified, squamous keratinizing epithelium is especially pronounced in the upper respiratory tract, and in the renal pelvis, urinary bladder, seminal vesicles, epididymis, prostate, salivary glands, and pancreas.

When there is deficiency of vitamin A, the intestinal flora is markedly changed as respects gram-negative and gram-positive bacteria in the faeces. The faeces of rats on the deficient diet are dry and hard, which may account for the disappearance of streptococci; otherwise there is no change in the proportion of bacteria which ferment glucose, lactose, and sucrose. The proportion of hydrogen-sulphide-forming bacteria remains constant.

Under deficiency of vitamin A, rats frequently die of bacterial invasion of the ear and nasal cavities before the appearance of ophthalmia. As the infection advances, it leads to nutritional disaster in which the animal is not restored to a normal condition by feeding rations containing vitamin A. Werkman has reported that a deficiency of vitamin A in the diet increased the susceptibility of rats to anthrax and pneumonia.

An interesting observation reported by Howe is the reversion of the odontoblasts to osteoblasts when animals are deprived of vitamin A. The odontoblastic membrane surrounds the pulp of the tooth and lies in apposition to the under surface of the dentine. From each odontoblast a fiber extends through a tubule in the dentine to the base of the enamel. The odontoblast forms dentine. Howe states that when animals are deprived of vitamin A, the odontoblasts revert to osteoblasts, or bone-forming cells, and that subsequently bone deposits may be formed by these cells. The frequent occurrence of pulp stones in the teeth of animals deprived of vitamin A supports this view. The importance of this vitamin for the health of the teeth appears, therefore, to be very great.

Vitamin B. Our knowledge of the specific effects of deficiency of vitamin B, which is one of several water-soluble nutrients, is less satisfactory than in the case of vitamin A, because uncomplicated vitamin B deficiency has less frequently been produced experimentally. By vitamin B we designate the anti-beriberi principle, or the anti-neuritic vitamin. There is little reason to doubt that deficiency of this vitamin is the cause of the disease beri-beri, which has taken millions of lives during the last 2000 years. The disease occurs mainly among rice-eating people who take polished rice as their principal food. Most of the vitamin is concentrated in the germ and the bran layer, both of which are removed in polishing. Beri-beri is still one of the chief causes of infant mortality in the Philippine Islands and in the East Indies.